Evidence map›Paper›PMID 24625978›Full record

ArticleCell death & disease2014

Aggrecan, link protein and tenascin-R are essential components of the perineuronal net to protect neurons against iron-induced oxidative stress.

A Suttkus, S Rohn, S Weigel, P Glöckner, T Arendt, M Morawski

Open access · goldAbstract readComparative Study
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

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36 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

A SuttkusUniversity of Leipzig, Department for Molecular and Cellular Mechanisms of Neurodegeneration, Paul Flechsig Institute for Brain Research, Jahnallee 59, Leipzig 04109, Germany.
S RohnUniversity of Leipzig, Department for Molecular and Cellular Mechanisms of Neurodegeneration, Paul Flechsig Institute for Brain Research, Jahnallee 59, Leipzig 04109, Germany.
S WeigelUniversity of Leipzig, Department for Molecular and Cellular Mechanisms of Neurodegeneration, Paul Flechsig Institute for Brain Research, Jahnallee 59, Leipzig 04109, Germany.
P GlöcknerUniversity of Leipzig, Department for Molecular and Cellular Mechanisms of Neurodegeneration, Paul Flechsig Institute for Brain Research, Jahnallee 59, Leipzig 04109, Germany.
T ArendtUniversity of Leipzig, Department for Molecular and Cellular Mechanisms of Neurodegeneration, Paul Flechsig Institute for Brain Research, Jahnallee 59, Leipzig 04109, Germany.
M Morawski1] University of Leipzig, Department for Molecular and Cellular Mechanisms of Neurodegeneration, Paul Flechsig Institute for Brain Research, Jahnallee 59, Leipzig 04109, Germany [2] SUNY Upstate Medical University, Department of Neuroscience and Physiology, WH 3240 750 East Adams Street, Syracuse, NY 13210, USA.
Leipzig University · DESUNY Upstate Medical University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Alzheimer's disease (AD), different types of neurons and different brain areas show differential patterns of vulnerability towards neurofibrillary degeneration, which provides the basis for a highly predictive profile of disease progression throughout the brain that now is widely accepted for neuropathological staging. In previous studies we could demonstrate that in AD cortical and subcortical neurons are constantly less frequently affected by neurofibrillary degeneration if they are enwrapped by a specialized form of the hyaluronan-based extracellular matrix (ECM), the so called 'perineuronal net' (PN). PNs are basically composed of large aggregating chondroitin sulphate proteoglycans connected to a hyaluronan backbone, stabilized by link proteins and cross-linked via tenascin-R (TN-R). Under experimental conditions in mice, PN-ensheathed neurons are better protected against iron-induced neurodegeneration than neurons without PN. Still, it remains unclear whether these neuroprotective effects are directly mediated by the PNs or are associated with some other mechanism in these neurons unrelated to PNs. To identify molecular components that essentially mediate the neuroprotective aspect on PN-ensheathed neurons, we comparatively analysed neuronal degeneration induced by a single injection of FeCl3 on four different mice knockout strains, each being deficient for a different component of PNs. Aggrecan, link protein and TN-R were identified to be essential for the neuroprotective properties of PN, whereas the contribution of brevican was negligible. Our findings indicate that the protection of PN-ensheathed neurons is directly mediated by the net structure and that both the high negative charge and the correct interaction of net components are essential for their neuroprotective function.

Indexed as

AggrecansAnimalsBrainBrevicanChloridesChondroitin SulfatesExtracellular MatrixExtracellular Matrix ProteinsFemaleFerric CompoundsGenotypeHyaluronic AcidMaleMiceMice, Inbred C57BLMice, KnockoutAcan protein, mouseAggrecansBcan protein, mouseBrevicanChloridesChondroitin SulfatesExtracellular Matrix Proteinsferric chlorideFerric CompoundsHyaluronic AcidProteoglycan Link ProteinProteoglycansTenascintenascin R

Identifiers

PMID24625978
PMCPMC3973247
OpenAlexW2022932966

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.